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Relevant bibliographies by topics / ADAM8

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Academic literature on the topic 'ADAM8'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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Journal articles on the topic "ADAM8"

1

Schlomann, Uwe, Kristina Dorzweiler, Elisa Nuti, Tiziano Tuccinardi, Armando Rossello, and Jörg W. Bartsch. "Metalloprotease inhibitor profiles of human ADAM8 in vitro and in cell-based assays." Biological Chemistry 400, no. 6 (June 26, 2019): 801–10. http://dx.doi.org/10.1515/hsz-2018-0396.

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AbstractADAM8 as a membrane-anchored metalloproteinase-disintegrin is upregulated under pathological conditions such as inflammation and cancer. As active sheddase, ADAM8 can cleave several membrane proteins, among them the low-affinity receptor FcεRII CD23. Hydroxamate-based inhibitors are routinely used to define relevant proteinases involved in ectodomain shedding of membrane proteins. However, for ADAM proteinases, common hydroxamates have variable profiles in their inhibition properties, commonly known for ADAM proteinases 9, 10 and 17. Here, we determined the inhibitor profile of human ADAM8 for eight ADAM/MMP inhibitors byin vitroassays using recombinant ADAM8 as well as thein vivoinhibition in cell-based assays using HEK293 cells to monitor the release of soluble CD23 by ADAM8. ADAM8 activity is inhibited by BB94 (Batimastat), GW280264, FC387 and FC143 (two ADAM17 inhibitors), made weaker by GM6001, TAPI2 and BB2516 (Marimastat), while no inhibition was observed for GI254023, an ADAM10 specific inhibitor. Modeling of inhibitor FC143 bound to the catalytic sites of ADAM8 and ADAM17 reveals similar geometries in the pharmacophoric regions of both proteinases, which is different in ADAM10 due to replacement in the S1 position of T300 (ADAM8) and T347 (ADAM17) by V327 (ADAM10). We conclude that ADAM8 inhibitors require maximum selectivity over ADAM17 to achieve specific ADAM8 inhibition.

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Conrad, Catharina, Julia Benzel, Kristina Dorzweiler, Lena Cook, Uwe Schlomann, Alexander Zarbock, Emily P. Slater, Christopher Nimsky, and Jörg W. Bartsch. "ADAM8 in invasive cancers: links to tumor progression, metastasis, and chemoresistance." Clinical Science 133, no. 1 (January 2019): 83–99. http://dx.doi.org/10.1042/cs20180906.

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Abstract Ectodomain shedding of extracellular and membrane proteins is of fundamental importance for cell–cell communication in neoplasias. A Disintegrin And Metalloproteinase (ADAM) proteases constitute a family of multifunctional, membrane-bound proteins with traditional sheddase functions. Their protumorigenic potential has been attributed to both, essential (ADAM10 and ADAM17) and ‘dispensable’ ADAM proteases (ADAM8, 9, 12, 15, and 19). Of specific interest in this review is the ADAM proteinase ADAM8 that has been identified as a significant player in aggressive malignancies including breast, pancreatic, and brain cancer. High expression levels of ADAM8 are associated with invasiveness and predict a poor patient outcome, indicating a prognostic and diagnostic potential of ADAM8. Current knowledge of substrates and interaction partners gave rise to the hypothesis that ADAM8 dysregulation affects diverse processes in tumor biology, attributable to different functional cores of the multidomain enzyme. Proteolytic degradation of extracellular matrix (ECM) components, cleavage of cell surface proteins, and subsequent release of soluble ectodomains promote cancer progression via induction of angiogenesis and metastasis. Moreover, there is increasing evidence for significance of a non-proteolytic function of ADAM8. With the disintegrin (DIS) domain ADAM8 binds integrins such as β1 integrin, thereby activating integrin signaling pathways. The cytoplasmic domain is critical for that activation and involves focal adhesion kinase (FAK), extracellular regulated kinase (ERK1/2), and protein kinase B (AKT/PKB) signaling, further contributing to cancer progression and mediating chemoresistance against first-line therapies. This review highlights the remarkable effects of ADAM8 in tumor biology, concluding that pharmacological inhibition of ADAM8 represents a promising therapeutic approach not only for monotherapy, but also for combinatorial therapies.

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Hall, Troii, Joseph W. Leone, Joseph F. Wiese, David W. Griggs, Lyle E. Pegg, Adele M. Pauley, Alfredo G. Tomasselli, and Marc D. Zack. "Autoactivation of human ADAM8: a novel pre-processing step is required for catalytic activity." Bioscience Reports 29, no. 4 (May 1, 2009): 217–28. http://dx.doi.org/10.1042/bsr20080145.

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Members of the ADAM (a disintegrin and metalloproteinase) family of proteins possess a multidomain architecture which permits functionalities as adhesion molecules, signalling intermediates and proteolytic enzymes. ADAM8 is found on immune cells and is induced by multiple pro-inflammatory stimuli suggesting a role in inflammation. Here we describe an activation mechanism for recombinant human ADAM8 that is independent from classical PC (pro-protein convertase)-mediated activation. N-terminal sequencing revealed that, unlike other ADAMs, ADAM8 undergoes pre-processing at Glu158, which fractures the Pro (pro-segment)-domain before terminal activation takes place to remove the putative cysteine switch (Cys167). ADAM8 lacking the DIS (disintegrin) and/or CR (cysteine-rich) and EGF (epidermal growth factor) domains displayed impaired ability to complete this event. Thus pre-processing of the Pro-domain is co-ordinated by DIS and CR/EGF domains. Furthermore, by placing an EK (enterokinase) recognition motif between the Pro- and catalytic domains of multiple constructs, we were able to artificially remove the pro-segment prior to pre-processing. In the absence of pre-processing of the Pro-domain a marked decrease in specific activity was observed with the autoactivated enzyme, suggesting that the Pro-domain continued to associate and inhibit active enzyme. Thus, pre-processing of the Pro-domain of human ADAM8 is important for enzyme maturation by preventing re-association of the pro-segment with the catalytic domain. Given the observed necessity of DIS and CR/EGF for pre-processing, we conclude that these domains are crucial for the proper activation and maturation of human ADAM8.

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Dreymueller, Daniela, Jessica Pruessmeyer, Julian Schumacher, Sandra Fellendorf, Franz Martin Hess, Anke Seifert, Aaron Babendreyer, Jörg W. Bartsch, and Andreas Ludwig. "The metalloproteinase ADAM8 promotes leukocyte recruitment in vitro and in acute lung inflammation." American Journal of Physiology-Lung Cellular and Molecular Physiology 313, no. 3 (September 1, 2017): L602—L614. http://dx.doi.org/10.1152/ajplung.00444.2016.

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Alveolar leukocyte recruitment is a hallmark of acute lung inflammation and involves transmigration of leukocytes through endothelial and epithelial layers. The disintegrin and metalloproteinase (ADAM) 8 is expressed on human isolated leukocytic cells and can be further upregulated on cultured endothelial and epithelial cells by proinflammatory cytokines. By shRNA-mediated knockdown we show that leukocytic ADAM8 is required on monocytic THP-1 cells for chemokine-induced chemotaxis as well as transendothelial and transepithelial migration. Furthermore, ADAM8 promotes αL-integrin upregulation and THP-1 cell adhesion to endothelial cells. On endothelial cells ADAM8 enhances transendothelial migration and increases cytokine-induced permeability. On epithelial cells the protease facilitates migration in a wound closure assay but does not affect transepithelial leukocyte migration. Blood leukocytes and bone marrow-derived macrophages (BMDM) from ADAM8-deficient mice show suppressed chemotactic response. Intranasal application of LPS to mice is accompanied with ADAM8 upregulation in the lung. In this model of acute lung inflammation ADAM8-deficient mice are protected against leukocyte infiltration. Finally, transfer experiments of BMDM in mice indicate that ADAM8 exerts a promigratory function predominantly on leukocytes. Our study provides in vitro and in vivo evidence that ADAM8 on leukocytes holds a proinflammatory function in acute lung inflammation by promoting alveolar leukocyte recruitment.

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Miyauchi, Masashi, Shunya Arai, Akira Honda, Sho Yamazaki, Keisuke Kataoka, Akihide Yoshimi, Kazuki Taoka, Keiki Kumano, and Mineo Kurokawa. "Patient-Derived Induced Pluripotent Stem Cells Revealed ADAM8/CD156 As a Novel Marker of TKI-Resistant Chronic Myeloid Leukemia Cells." Blood 128, no. 22 (December 2, 2016): 1878. http://dx.doi.org/10.1182/blood.v128.22.1878.1878.

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Abstract Since the emergence of tyrosine kinase inhibitors (TKIs), long-term survival of patients with chronic myelogenous leukemia (CML) has been improved. However, those TKIs have not fully succeeded in curing CML, mainly due to TKI-resistant CML stem cells. CML stem cells are often difficult to analyze because they represent an extremely minor population of CML cells. To overcome this obstacle, we established integration-free induced pluripotent stem cells (iPSCs) from bone marrow (BM) cells of two patients with CML in chronic phase (CML-CP) and obtained CML pre-hematopoietic progenitor cells (CML-pre-HPCs), immature hematopoietic cells phenotypically defined by CD34+/CD45-/CD43+ cells. In semisolid and liquid cultures, CML-pre-HPCs recapitulated the principal features of CML stem cells, multi-potency and the resistance against imatinib. Gene expression enrichment analysis for CML-pre-HPCs demonstrated that several gene sets, including those related to the maintenance of hematopoietic stem cells were enriched. In addition, we found that a disintegrin and metalloprotease 8 (ADAM8), also known as CD156, was highly enhanced in CML-pre-HPCs and the expression level of ADAM8 was even increased after the treatment of imatinib in vitro. To address the significance of ADAM8 in CMP-CP patient, we evaluated purified ADAM8+ cells by fluorescence-activated cell sorting (FACS) in primary samples. First, FACS analysis found that ADAM8+ cells were enriched more in BM samples of patient with newly diagnosed CML-CP than normal or other types of leukemias among CD34+ fraction. ADAM8+ cells were enriched in CD34+/CD38- fraction compaered to CD34+/38+ fraction in BM of CML-CP patients, indicating that ADMA8+ cells represent immature hematopietic cells. In cell viability assays, ADAM8+/CD38+ CML cells in newly diagnosed CML-CP patient enhibited imatinib-resistance and imatinib-induced apoptosis in vitro was strongly suppressed in ADAM8+ CML cells compared to ADAM8- cells. Even in CD34+/CD38+ fraction, which was previously known as TKI-sensitive fraction, ADAM8+ cells exhibited TKI-resistance in both cell viability and apoptosis assay, indicating that ADAM8 would be a useful marker of TKI-resistant CML cells. Finally, to evaluate the significance of ADAM8 as a marker of TKI-resistant CML cells in vivo, we measured the frequency of CML cells in BM samples of CML-CP patients who had achieved major or complete molecular response (MMR; n = 2 or CMR; n = 1) after the administration of TKIs by limiting dilution analysis. In CML patients with MMR, CML cells remained in ADAM8+ cells at higher frequency in spite of steep decline of CML cells in ADAM8- cells The frequency of CML cells was as high in CD34+/CD38+/ADAM8+ fraction as in CD34+/38- CML stem cell fraction. Even in a patient with CMR, residual CML cells were detected in ADAM8+ population among CD34+/CD38+ fraction, whereas CML cells were undetectable in ADAM8- population. In conclusion, we have established a powerful platform with CML-iPSCs to investigate the pathophysiology of TKI-resistant CML stem cells. Using this platform, we have identified ADAM8 as a novel marker of TKI-resistant CML cells. CD34+/CD38+/ADAM8+ fraction, as well as CD34+/CD38- fraction, was an important population that defines residual CML cells even in CML-CP patients with deep molecular response after the treatment of TKI. ADAM8 would become an attractive candidate of novel therapeutic targets against TKI-resistant CML cells. Disclosures Kataoka: Yakult: Honoraria; Boehringer Ingelheim: Honoraria; Kyowa Hakko Kirin: Honoraria.

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Qi, Bing, Han Liu, Ying Dong, Xueying Shi, Qi Zhou, Fen Zeng, Nabuqi Bao, et al. "The nine ADAMs family members serve as potential biomarkers for immune infiltration in pancreatic adenocarcinoma." PeerJ 8 (September 30, 2020): e9736. http://dx.doi.org/10.7717/peerj.9736.

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Background The functional significance of ADAMs family members in the immune infiltration of pancreatic adenocarcinoma (PAAD) awaits elucidation. Methods ADAMs family members with significant expression were identified among differentially expressed genes of PAAD based on The Cancer Genome Atlas (TCGA) database followed by a verification based on the Oncomine database. The correlation of ADAMs in PAAD was estimated with the Spearman’s rho value. The pathway enrichment of ADAMs was performed by STRING and GSEALite, respectively. The protein–protein interaction and Gene Ontology analyses of ADAMs and their similar genes were exanimated in STRING and visualized by Cytoscape. Subsequently, the Box-Whisker plot was used to show a correlation between ADAMs and different tumor grade 1/2/3/4 with Student’s t-test. TIMER was applied to estimate a correlation of ADAMs expressions with immune infiltrates and immune checkpoint blockade (ICB) immunotherapy-related molecules. Furthermore, the effect of copy number variation (CNV) of ADAMs genes was assessed on the immune infiltration levels. Result ADAM8/9/10/12/15/19/28/TS2/TS12 were over-expressed in PAAD. Most of the nine ADAMs had a significant correlation. ADAM8/12/15/19 expression was remarkably increased in the comparison between grade 1 and grade 2/3 of PAAD. ADAM8/9/10/12/19/28/TS2/TS12 had a positive correlation with almost five immune infiltrates. ADAM12/19/TS2/TS12 dramatically related with ICB immunotherapy-related molecules. CNV of ADAMs genes potentially influenced the immune infiltration levels. Conclusion Knowledge of the expression level of the ADAMs family could provide a reasonable strategy for improved immunotherapies to PAAD.

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Łukaszewicz-Zając, Marta, Maciej Dulewicz, and Barbara Mroczko. "A Disintegrin and Metalloproteinase (ADAM) Family: Their Significance in Malignant Tumors of the Central Nervous System (CNS)." International Journal of Molecular Sciences 22, no. 19 (September 26, 2021): 10378. http://dx.doi.org/10.3390/ijms221910378.

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Despite the considerable advances in diagnostic methods in medicine, central nervous system (CNS) tumors, particularly the most common ones—gliomas—remain incurable, with similar incidence rates and mortality. A growing body of literature has revealed that degradation of the extracellular matrix by matrix metalloproteinases (MMPs) might be involved in the pathogenesis of CNS tumors. However, the subfamily of MMPs, known as disintegrin and metalloproteinase (ADAM) proteins are unique due to both adhesive and proteolytic activities. The objective of our review is to present the role of ADAMs in CNS tumors, particularly their involvement in the development of malignant gliomas. Moreover, we focus on the diagnostic and prognostic significance of selected ADAMs in patients with these neoplasms. It has been proven that ADAM12, ADAMTS4 and 5 are implicated in the proliferation and invasion of glioma cells. In addition, ADAM8 and ADAM19 are correlated with the invasive activity of glioma cells and unfavorable survival, while ADAM9, -10 and -17 are associated with tumor grade and histological type of gliomas and can be used as prognostic factors. In conclusion, several ADAMs might serve as potential diagnostic and prognostic biomarkers as well as therapeutic targets for malignant CNS tumors. However, future research on ADAMs biology should be performed to elucidate new strategies for tumor diagnosis and treatment of patients with these malignancies.

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Jaworek, Christian, Yesim Verel-Yilmaz, Sarah Driesch, Sarah Ostgathe, Lena Cook, Steffen Wagner, Detlef K. Bartsch, Emily P. Slater, and Jörg W. Bartsch. "Cohort Analysis of ADAM8 Expression in the PDAC Tumor Stroma." Journal of Personalized Medicine 11, no. 2 (February 10, 2021): 113. http://dx.doi.org/10.3390/jpm11020113.

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Pancreatic ductal adenocarcinoma (PDAC) is a cancer type with one of the highest mortalities. The metalloprotease-disintegrin ADAM8 is highly expressed in pancreatic cancer cells and is correlated with an unfavorable patient prognosis. However, no information is available on ADAM8 expression in cells of the tumor microenvironment. We used immunohistochemistry (IHC) to describe the stromal cell types expressing ADAM8 in PDAC patients using a cohort of 72 PDAC patients. We found ADAM8 expressed significantly in macrophages (6%), natural killer cells (40%), and neutrophils (63%), which showed the highest percentage of ADAM8 expressing stromal cells. We quantified the amount of ADAM8+ neutrophils in post-capillary venules in PDAC sections by IHC. Notably, the amount of ADAM8+ neutrophils could be correlated with post-operative patient survival times. In contrast, neither the total neutrophil count in peripheral blood nor the neutrophil-to-lymphocyte ratio showed a comparable correlation. We conclude from our data that ADAM8 is, in addition to high expression levels in tumor cells, present in tumor-associated stromal macrophages, NK cells, and neutrophils and, in addition to functional implications, the ADAM8-expressing neutrophil density in post-capillary venules is a diagnostic parameter for PDAC patients when the numbers of ADAM8+ neutrophils are quantified.

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Awan, Tanzeela, Aaron Babendreyer, Justyna Wozniak, Abid Mahmood Alvi, Viktor Sterzer, Lena Cook, Jörg W. Bartsch, Christian Liedtke, Daniela Yildiz, and Andreas Ludwig. "Expression of the Metalloproteinase ADAM8 Is Upregulated in Liver Inflammation Models and Enhances Cytokine Release In Vitro." Mediators of Inflammation 2021 (March 11, 2021): 1–15. http://dx.doi.org/10.1155/2021/6665028.

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Acute and chronic liver inflammation is driven by cytokine and chemokine release from various cell types in the liver. Here, we report that the induction of inflammatory mediators is associated with a yet undescribed upregulation of the metalloproteinase ADAM8 in different murine hepatitis models. We further show the importance of ADAM8 expression for the production of inflammatory mediators in cultured liver cells. As a model of acute inflammation, we investigated liver tissue from lipopolysaccharide- (LPS-) treated mice in which ADAM8 expression was markedly upregulated compared to control mice. In vitro, stimulation with LPS enhanced ADAM8 expression in murine and human endothelial and hepatoma cell lines as well as in primary murine hepatocytes. The enhanced ADAM8 expression was associated with an upregulation of TNF-α and IL-6 expression and release. Inhibition studies indicate that the cytokine response of hepatoma cells to LPS depends on the activity of ADAM8 and that signalling by TNF-α can contribute to these ADAM8-dependent effects. The role of ADAM8 was further confirmed with primary hepatocytes from ADAM8 knockout mice in which TNF-α and IL-6 induction and release were considerably attenuated. As a model of chronic liver injury, we studied liver tissue from mice undergoing high-fat diet-induced steatohepatitis and again observed upregulation of ADAM8 mRNA expression compared to healthy controls. In vitro, ADAM8 expression was upregulated in hepatoma, endothelial, and stellate cell lines by various mediators of steatohepatitis including fatty acid (linoleic-oleic acid), IL-1β, TNF-α, IFN-γ, and TGF-β. Upregulation of ADAM8 was associated with the induction and release of proinflammatory cytokines (TNF-α and IL-6) and chemokines (CX3CL1). Finally, knockdown of ADAM8 expression in all tested cell types attenuated the release of these mediators. Thus, ADAM8 is upregulated in acute and chronic liver inflammation and is able to promote inflammation by enhancing expression and release of inflammatory mediators.

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Dreymueller, Daniela, Stefan Uhlig, and Andreas Ludwig. "ADAM-family metalloproteinases in lung inflammation: potential therapeutic targets." American Journal of Physiology-Lung Cellular and Molecular Physiology 308, no. 4 (February 15, 2015): L325—L343. http://dx.doi.org/10.1152/ajplung.00294.2014.

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Acute and chronic lung inflammation is driven and controlled by several endogenous mediators that undergo proteolytic conversion from surface-expressed proteins to soluble variants by a disintegrin and metalloproteinase (ADAM)-family members. TNF and epidermal growth factor receptor ligands are just some of the many substrates by which these proteases regulate inflammatory or regenerative processes in the lung. ADAM10 and ADAM17 are the most prominent members of this protease family. They are constitutively expressed in most lung cells and, as recent research has shown, are the pivotal shedding enzymes mediating acute lung inflammation in a cell-specific manner. ADAM17 promotes endothelial and epithelial permeability, transendothelial leukocyte migration, and inflammatory mediator production by smooth muscle and epithelial cells. ADAM10 is critical for leukocyte migration and alveolar leukocyte recruitment. ADAM10 also promotes allergic asthma by driving B cell responses. Additionally, ADAM10 acts as a receptor for Staphylococcus aureus ( S. aureus) α-toxin and is crucial for bacterial virulence. ADAM8, ADAM9, ADAM15, and ADAM33 are upregulated during acute or chronic lung inflammation, and recent functional or genetic analyses have linked them to disease development. Pharmacological inhibitors that allow us to locally or systemically target and differentiate ADAM-family members in the lung suppress acute and asthmatic inflammatory responses and S. aureus virulence. These promising results encourage further research to develop therapeutic strategies based on selected ADAMs. These studies need also to address the role of the ADAMs in repair and regeneration in the lung to identify further therapeutic opportunities and possible side effects.

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Dissertations / Theses on the topic "ADAM8"

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Nishimura, Daigo. "Roles of ADAM8 in elimination of injured muscle fibers prior to skeletal muscle regeneration." Kyoto University, 2015. http://hdl.handle.net/2433/199212.

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Sasko, Eric [Verfasser], and Udo [Akademischer Betreuer] Bakowsky. "Entwicklung und Charakterisierung echogener Liposomen zur Targetierung von ADAM8 / Eric Sasko ; Betreuer: Udo Bakowsky." Marburg : Philipps-Universität Marburg, 2017. http://d-nb.info/1135385599/34.

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Yu, Xiangdi [Verfasser], and Jörg W. [Akademischer Betreuer] Bartsch. "Purification and Functional Characterization of Recombinant Human ADAM8 protease / Xiangdi Yu. Betreuer: Jörg W. Bartsch." Marburg : Philipps-Universität Marburg, 2015. http://d-nb.info/1071947788/34.

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Liang, Jingjing. "Toxicity and Processing of Cellular Prion Protein in Skeletal Muscles." Case Western Reserve University School of Graduate Studies / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=case1323450797.

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Heß, Franz Martin [Verfasser]. "The role of the metalloproteases ADAM8, 9, 10 and 17 in leukocyte migration in vitro / Franz Martin Heß." Aachen : Hochschulbibliothek der Rheinisch-Westfälischen Technischen Hochschule Aachen, 2013. http://d-nb.info/1037046021/34.

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Schicktanz, Hanka Iris [Verfasser]. "Immunhistochemische Expressionsanalyse von RECK, ADAM8, CD146 und COX-2 auf ihre Eignung als Prognosemarker des Prostatakarzinoms / Hanka Iris Schicktanz." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2010. http://d-nb.info/1024364720/34.

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Richens, Joanna. "Expression of ADAM8 on cells of the immune system and potential modulation by the mite allergen Der p 1." Thesis, University of Nottingham, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.438327.

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Schumacher, Julian Verfasser], Andreas [Akademischer Betreuer] Ludwig, and Gabriele [Akademischer Betreuer] [Pradel. "Role of the proteases ADAM8, ADAM10 and ADAM17 in bleomycin induced lung inflammation / Julian Schumacher ; Andreas Ludwig, Gabriele Pradel." Aachen : Universitätsbibliothek der RWTH Aachen, 2018. http://d-nb.info/1169915183/34.

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Schumacher, Julian [Verfasser], Andreas Akademischer Betreuer] Ludwig, and Gabriele [Akademischer Betreuer] [Pradel. "Role of the proteases ADAM8, ADAM10 and ADAM17 in bleomycin induced lung inflammation / Julian Schumacher ; Andreas Ludwig, Gabriele Pradel." Aachen : Universitätsbibliothek der RWTH Aachen, 2018. http://d-nb.info/1169915183/34.

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Awan, Tanzeela Verfasser], Andreas [Akademischer Betreuer] Ludwig, Gabriele [Akademischer Betreuer] [Pradel, and Martin [Akademischer Betreuer] Zenke. "Role and regulation of the metalloproteinase ADAM8 in liver inflammation and hepatocellular carcinoma / Tanzeela Awan ; Andreas Ludwig, Gabriele Pradel, Martin Zenke." Aachen : Universitätsbibliothek der RWTH Aachen, 2021. http://d-nb.info/1227992858/34.

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Books on the topic "ADAM8"

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Toshokan, Ōsaka Daigaku. A collection of Adam Smith =: [Adamu Sumisu korekushon]. [Osaka]: Osaka University Library, 1990.

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Mkrtchʻyan, Satʻenik. Merk inchʻpes Adamě: Gol kak Adam : ōrorotsʻayin deṛ chʻtsnvats mankan hamar. Erevan: "Van Aryan", 2013.

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Democracy, equality, and justice: John Adams, Adam Smith, and political economy. Lanham, MD: Lexington Books, 2007.

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Wawrzykowska-Wierciochowa, Dionizja. Adam i Maryla: Dzieje romantycznej miłości Adama Mickiewicza i Maryli Wereszczakówny. Warszawa: Instytut Wydawniczy Związków Zawodowych, 1990.

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Adam Smith and the classics: The classical heritage in Adams Smith's thought. Oxford [England]: Oxford University Press, 2001.

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Hill, John E. Revolutionary values for a new millennium: John Adams, Adam Smith, and social virtue. Lanham, Md: Lexington Books, 1999.

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Głowacki, Zbigniew. Księdza Adama Ludwika Szafrańskiego teologia liturgii: Rev. Adam Ludwik Szafrański's theology of liturgy. Lublin: Wydawnictwo KUL, 2013.

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Haidegger, Christine. Adam/Adam: Roman. [Wien]: Verlag der Österreichischen Staatsdruckerei, 1987.

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Adam/Adam: Roman. [Wien]: Verlag der Österreichischen Staatsdruckerei, 1985.

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Adami, Valerio. Adami. Edited by Boldrini Maurizio 1958-, Civai Mauro, Palazzo pubblico (Siena Italy), and Siena (Italy). Assessorato alla cultura. [Siena, Italy]: Editori senesi, 1994.

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Book chapters on the topic "ADAM8"

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Pattinson, Shaun D. "Adams." In Revisiting Landmark Cases in Medical Law, 28–53. Abingdon, Oxon [UK] ; New York, NY : Routledge, 2018. | Series: Biomedical Law and Ethics Library: Routledge, 2018. http://dx.doi.org/10.4324/9781315750651-2.

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Levin, Michael. "John Adams." In The Spectre of Democracy, 71–90. London: Palgrave Macmillan UK, 1992. http://dx.doi.org/10.1007/978-1-349-12547-0_3.

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Hogan, Margaret A. "Abigail Adams." In A Companion to First Ladies, 20–37. Hoboken, NJ: John Wiley & Sons, Inc, 2016. http://dx.doi.org/10.1002/9781118732250.ch2.

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Bernstein, R. B. "John Adams." In A Companion to John Adams and John Quincy Adams, 3–35. Oxford: John Wiley & Sons, 2013. http://dx.doi.org/10.1002/9781118524381.ch1.

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Hogan, Margaret A. "Abigail Adams." In A Companion to John Adams and John Quincy Adams, 218–38. Oxford: John Wiley & Sons, 2013. http://dx.doi.org/10.1002/9781118524381.ch11.

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Strasen, Sven. "Adams, Douglas." In Kindlers Literatur Lexikon (KLL), 1. Stuttgart: J.B. Metzler, 2020. http://dx.doi.org/10.1007/978-3-476-05728-0_7858-1.

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Steimle, Josh. "Patrick Adams." In Chief Marketing Officers at Work, 67–78. Berkeley, CA: Apress, 2016. http://dx.doi.org/10.1007/978-1-4842-1931-7_7.

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Hellegers, Desiree. "Arnette Adams." In No Room of Her Own, 165–72. New York: Palgrave Macmillan US, 2011. http://dx.doi.org/10.1057/9780230339200_15.

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Sanchez-Behar, Alexander. "Introduction." In John Adams, 1–5. New York : Routledge, 2020. | Series: Routledge music bibliographies: Routledge, 2020. http://dx.doi.org/10.4324/9781315165714-1.

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Sanchez-Behar, Alexander. "Other Internet Sources." In John Adams, 151–58. New York : Routledge, 2020. | Series: Routledge music bibliographies: Routledge, 2020. http://dx.doi.org/10.4324/9781315165714-10.

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Conference papers on the topic "ADAM8"

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Li, San-Qiang, Hong-Ye Meng, Shou-Min Xi, Ling-Jun Ma, and Wu-BiaoYang. "Expression of ADAM8 in Liver Cancer." In 2012 International Conference on Biomedical Engineering and Biotechnology (iCBEB). IEEE, 2012. http://dx.doi.org/10.1109/icbeb.2012.210.

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Cataldo, D. D., C. Sepult, C. Vanwinge, A. Gillard, B. Duysinx, E. Maquoi, C. Poulet, A. Debit, A. Noel, and M. Bellefroid. "Role of ADAM8 Protease in Malignant Pleural Mesothelioma Chemoresistance." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4206.

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Knolle, MD, and CA Owen. "ADAM8 Limits Allergic Airway Inflammation in Mice by Increasing Macrophage Apoptosis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2234.

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Dreymueller, Daniela, Jessica Pruessmeyer, Julian Schumacher, Joerg W. Bartsch, and Andreas Ludwig. "LATE-BREAKING ABSTRACT: The metalloproteinase ADAM8 promotes acute and chronic lung inflammation." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa3908.

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Deng, Linhong, Jun Chen, Jiaoyue Long, Yiyuan Duan, Xuemei Jiang, and Rong Xu. "ADAM8 Inhibitor Peptide Reduces Inflammation And Bronchial Hyperresponsivess In Ovalbumin-Sensitized Mice." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2762.

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Das, Sonia G., Stefania Pianetti, Gail E. Sonenshein, and Nora D. Mineva. "Abstract 23: Antibody targeting of ADAM8 for treatment of triple-negative breast cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-23.

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Li, San-Qiang, Hong-Ye Meng, Shou-Min Xi, Ling-Jun Ma, and Wu-Biao Yang. "The Effect of CCl4-induced Acute Liver Injury on the ADAM8 Expression in the Mice." In 2012 International Conference on Biomedical Engineering and Biotechnology (iCBEB). IEEE, 2012. http://dx.doi.org/10.1109/icbeb.2012.415.

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Romagnoli, Mathilde, Nora D. Mineva, Delphine Loussouarn, Sophie Barillé-Nion, Mike Polmear, Irene Georgakoudi, Catharina Conrad, et al. "Abstract B62: ADAM8 promotes tumorigenesis, angiogenesis, and spreading of circulating tumor cells in breast cancer." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-b62.

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Das, Sonia G., Mathilde Romagnoli, Nora D. Mineva, and Gail E. Sonenshein. "Abstract B166: MicroRNAs downstream of ADAM8 as therapeutic targets and non-invasive biomarkers for triple-negative breast cancer." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b166.

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Romagnoli, Mathilde, Stefania Pianetti, Sonia G. Das, Delphine Loussouarn, Carole Gourmelon, Mario Campone, Sophie Barillé-Nion, et al. "Abstract 1137: ADAM8 drives aggressive phenotype of triple-negative inflammatory breast cancer & constitutes a novel therapeutic target." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1137.

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Reports on the topic "ADAM8"

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Heeringa, Steven, Gwenith Fisher, Michael Hurd, Kenneth Langa, Mary Beth Ofstedal, Brenda Plassman, and Willard Rodgers. ADAMS: Sample Design, Weighting and Analysis for ADAMS. Institute for Social Research, University of Michigan, 2009. http://dx.doi.org/10.7826/isr-um.06.585031.001.05.0019.2009.

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Klumpp, C. L., and J. L. Pfaltz. Implementation of an ADAMS prototype: the ADAMS preprocessor (AP). Office of Scientific and Technical Information (OSTI), August 1988. http://dx.doi.org/10.2172/6265085.

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Pfaltz, J. L., J. C. French, A. Grimshaw, Sang H. Son, P. Baron, S. Janet, A. Kim, C. Klumpp, Yi Lin, and L. Lloyd. The ADAMS database language. Office of Scientific and Technical Information (OSTI), February 1989. http://dx.doi.org/10.2172/6062396.

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Pfaltz, J. L., J. C. French, and J. L. Whitlatch. Scoping persistent name spaces in ADAMS. Office of Scientific and Technical Information (OSTI), June 1988. http://dx.doi.org/10.2172/6163935.

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Thompson, Hugh, Salvatore J. Stolfo, Angelos D. Keromytis, and Shlomo Hershkop. Anomaly Detection at Multiple Scales (ADAMS). Fort Belvoir, VA: Defense Technical Information Center, November 2011. http://dx.doi.org/10.21236/ada552461.

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Chaturvedi, Arvind. Engineering Soils Map of Adams County, Indiana. West Lafayette, IN: Purdue University, 1989. http://dx.doi.org/10.5703/1288284314176.

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Korosec, M. A. Geologic map of the Mount Adams Quadrangle, Washington. Office of Scientific and Technical Information (OSTI), January 1987. http://dx.doi.org/10.2172/6325892.

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Ali, Alee. ADAM Program Execution Plan LANL Inputs (FY2022). Office of Scientific and Technical Information (OSTI), August 2021. http://dx.doi.org/10.2172/1814729.

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Burton, Jacqueline C. Final phase II report : QuickSite® investigation, Adams, Nebraska. Office of Scientific and Technical Information (OSTI), October 2002. http://dx.doi.org/10.2172/1188315.

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MORRISON KNUDSEN ENGINEERS INC DENVER CO. Aquatic Resources of Rocky Mountain Arsenal Adams County, Colorado. Fort Belvoir, VA: Defense Technical Information Center, September 1989. http://dx.doi.org/10.21236/ada272102.

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